RESP Flashcards

1
Q

A 2.8cm pneumothorax is identified. The patient is symptomatic but haemodynamically stable. Presence of what would indicate immediate chest drain rather than aspiration?

A

Bilateral pneumothoraces

Underlying lung disease

Significant hypoxia

> 50 years old with significant smoking history

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2
Q

Acronym for upper zone fibrosis:

A

CHARTS

Coal worker’s pneumoconiosis

Histiocytosis / hypersensitivity pneumonitis

Ankylosing spondylitis

Radiation

Tuberculosis

Silicosis / sarcoidosis

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3
Q

What is the proposed mechanism of mitral stenosis causing haemoptysis?

A

Secondary to rupture of the bronchial veins caused by left atrial pressure.

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4
Q

Combination of which 3 symptoms is a classical presentation of GPA?

A

Haemoptysis - pulmonary haemorrhage

Renal impairment - RPGN

Flat / saddle nose - due to collapse of the nasal septum

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5
Q

What are the 2 most common causes of bilateral hilar lymphadenopathy?

A

Sarcoidosis
TB

Others include lymphoma, pneumoconiois and fungi e.g. histoplasmosis, coccidioidomyocosis

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6
Q

Bilateral hilar lymphadenopathy in combination with which 3 other symptoms would be a typical presentation of sarcoidosis?

A

Cough

Low grade fever

Erythema nodosum, lymphadenopathy

Afro-Caribbean descent is much more common!

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7
Q

What abnormalities may you observe on lung function testing of obese patients?

A

Reduced FEV1
Reduced FVC
Normal FEV1/FVC ratio

Reduced expiratory reserve volume

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8
Q

Fibrosis causes predominantly affecting the lower zones:

A

ACID

Asbestos

Connective tissue disorders; RA/SLE/Sjogren’s

Idiopathic

Drug induced e.g. amiodarone, bleomycin, methotrexate

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9
Q

What does bronchiectasis describe?

A

Permanent dilatation of the airways secondary to chronic infection or inflammation

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10
Q

What are some causes of bronchiectasis?

A

Post-infectious: severe bacterial e.g. pertussis or TB, viral inc measles, fungal causing damage to bronchial walls.

Systemic: RA, Sjogren’s, IBD, vasculitis e.g. GPA

Congenital and genetic: primary ciliary dyskinesia (Kartagener’s), CF

Idiopathic

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11
Q

State the 4 most common organisms in bronchiectasis:

A

Haemophilus influenzae

Pseudomonas aeruginosa

Klebsiella

Strep pneumoniae

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12
Q

After assessing for treatable causes of bronchiectasis, what management options are available?

A

Physical inspiratory muscle training (works in non-CF bronchiectasis)

Antibiotics for exacerbations

Bronchodilators can sometimes have a role

Immunisations are key

Surgery in selected cases

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13
Q

What is cor pulmonale?

A

Right sided heart failure caused by pulmonary hypertension.

Back pressure into the systemic venous system.

Main presenting complaint = shortness of breath
Peripheral oedema
Increased SOB
Chest pain

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14
Q

Causes of cor pulmonale:

A

COPD
PE
Interstitial lung disease
CF
Primary Pulmonary Hypertension

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15
Q

Signs of cor pulmonale:

A

Hypoxia
Raised JVP
Cyanosis
Peripheral oedema
Third heart sound
Murmur
Tricuspid regurgitation = pansystolic
Hepatomegaly (?pulsatile hepatomegaly)

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16
Q

Management of cor pulmonale:

A

Treat symptoms and underlying cause

Prognosis is poor unless reversible cause, otherwise it is a late stage condition.

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17
Q

Which 3 underlying lesions can result in Eisenmenger syndrome?

A

Atrial septal defect

Ventricular septal defect

PDA

18
Q

Describe the pathophysiology of Eisenmenger’s syndrome.

A

Left to right shunt occur due to higher pressure in the left side of the heart. Blood still travels to the lungs from the RV so patients do not become cyanotic.

Over time, if the defect is not corrected then a RIGHT TO LEFT shunt can occur. This is due to the extra blood flowing into the right side of the heart and lungs increases pressure in the pulmonary vessels, causing pulmonary hypertension. When pulmonary pressure exceeds systemic pressure, a right to left shunt occurs, bypassing the lungs and results in circulation of deoxygenated blood.

19
Q

What is the body’s compensatory mechanism for Eisenmenger’s syndrome?

A

Bone marrow induced more erythropoeisis, resulting in polycythaemia (high conc of Hb in the blood).

Polycythaemia gives a plethoric complexion, increases plasma viscosity and increases risk of thrombus formation.

20
Q

State the 3 types of ANCA-associated vasculitis, and which type of ANCA they present with. They are all small vessel vasculitides.

A

GPA - cANCA

Microscopic polyangiitis - pANCA

Eosinophilic granulomatosis with polyangiitis - pANCA

21
Q

Which parts of the body does GPA affect?

A

Upper and lower respiratory tract

Kidneys (RPGN)

22
Q

Describe a clinical picture of someone presenting with GPA.

A

Nose bleeds
Sinusitis
Cough, wheeze, haemoptysis
Saddle shaped nose

RPGN

23
Q

Which condition can present with severe asthma, onset in middle age?

A

Eosinophilic granulomatosis with polyangiitis.

24
Q

What is lupus pernio and which condition is is associated with?

A

Raised purple skin lesions on cheeks and nose

Associated with sarcoidosis!

25
Q

Sarcoidosis is characterised by the presence of non-caseating granulomas.
Discuss the prognosis of sarcoidosis.

A

Spontaneously resolves in around half of patients, usually within 2 years.

In some patients it progresses to pulmonary fibrosis and pulmonary hypertension.

26
Q

Which blood tests are used to screen / look for sarcoidosis when suspected?

A

serum ACE; HIGH

Calcium; low

27
Q

What does Lofgren’s syndrome refer to?

A

An acute form of sarcoidosis

Erythema nodosum

Bilateral hilar lymphadenopathy

Polyarthralgia

Fever

28
Q

Conservative management for sarcoidosis is considered in patients with mild or no symptoms. What is the first and second line for patients who do require input?

A

Oral steroids 6-24 months + bisphosphonates

Methotrexate 2nd line

29
Q

Sarcoidosis can affect any organ in the body, but the lungs are most commonly affected, in up to 90% of patients. Discuss some manifestations of sarcoidosis, split into respiratory, systemic, eye, liver, renal, heart, CNS, PNS and bones

A

https://zerotofinals.com/medicine/respiratory/sarcoidosis/

30
Q

Why does hypercalcaemia occur in sarcoidosis?

A

Macrophages inside the granulomas cause increased conversion of vitamin D to its active form of 1,25-dihydroxycholecalciferol.

31
Q

What acute feature of sarcoidosis does it share with malaria?

A

Swinging / cyclical fever

32
Q

What does Heerfordt’s syndrome refer to?

A

Parotid enlargement, fever and uveitis secondary to sarcoidosis.

33
Q

Describe the usefulness of ACE levels in sarcoidosis.

A

Sensitivity of 60% and specificity of 70%, so are not reliable in diagnostic terms, but can have a role in monitoring disease activity.

34
Q

Discuss the stages of sarcoidosis as rated from a chest x-ray.

A

Stage 0 = normal

Stage 1 = bilateral hilar lymphadenopathy

Stage 2 = BHL + interstitial infiltrates

Stage 3 = Diffuse interstitial infiltrates only

Stage 4 = Diffuse fibrosis

35
Q

What are the clinical indications for steroid treatment in sarcoidosis?

A

CXR Stage 2 or 3 with symptoms

Hypercalcaemia (occurs in 10% of patients)

Eye, heart or neuro involvement

36
Q

Give 5 factors associated with poor prognosis in sarcoidosis.

A

CXR stage III or IV features

Absence of erythema nodosum

Presence of extrapulmonary manifestation e.g. lupus pernio, splenomegaly

Insidious onset, symptoms for > 6 months

Black African or Afro-Caribbean ethnicity

37
Q

What does ABPA stand for, and how is it treated?

A

Allergic bronchopulmonary aspergillosis

Due to excessive immune response

1st line = STEROIDS PO
Adjunct = antifungal therapy e.g. itraconazole

38
Q

Dextrocardia in combination with bronchiectasis is highly suggestive of:

A

Kartagener’s syndrome

39
Q

CXR appearance of asbestosis:

A

Patchy lower zone fibrosis

Pleural plaques

40
Q

What is the MOA for varenicline?

A

Nicotinic receptor partial agonist

41
Q

What is the MOA of bupropion?

A

Norepinephrine-dopamine reuptake inhibitor and nicotinic antagonist